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Art. -Nr.: HY-187225

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NCP07

NCP07 is a PROTAC degrader targeting the coactivator-binding site (CBS) of ERα. NCP07 induces the formation of the ERα-NCP07-VHL ternary complex and promotes ERα degradation via the ubiquitin-proteasome system. NCP07 induces apoptosis and cell cycle arrest in endocrine therapy-resistant breast cancer cells. NCP07 inhibits the proliferation of wild-type and ESR1-mutant breast cancer cells. NCP07 is applicable to breast cancer-related research.
(Pink: ERα Target protein ligand; Blue: VHL ligand (HY-112078); Black: linker (HY-N0067)).

Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.

Formel: C₅₈H₇₂N₈O₁₃S
Molecular Weight:1121.30

Speicherung:

Please store the product under the recommended conditions in the Certificate of Analysis.

NCP07 Chemical Structure

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Use of MCE Products

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biologische Aktivität
- Beschreibung
- IC₅₀ & Target
- In Vitro
- In Vivo
Chemical Information
Reinheit & Dokumentation
Verweise
Calculators
Help & FAQs
Classifications
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Biologische Aktivität

Beschreibung

NCP07 is a PROTAC degrader targeting the coactivator-binding site (CBS) of ERα. NCP07 induces the formation of the ERα-NCP07-VHL ternary complex and promotes ERα degradation via the ubiquitin-proteasome system. NCP07 induces apoptosis and cell cycle arrest in endocrine therapy-resistant breast cancer cells. NCP07 inhibits the proliferation of wild-type and ESR1-mutant breast cancer cells. NCP07 is applicable to breast cancer-related research^[1]. (Pink: ERα Target protein ligand; Blue: VHL ligand (HY-112078); Black: linker (HY-N0067)).

IC₅₀ & Target

^[1]

ERα

Alle PROTACs Isoform-spezifische Produkte anzeigen :

Alle Estrogen Receptor/ERR Isoform-spezifische Produkte anzeigen :

In Vitro

Anti-cancerApoptosisCell Cycle Regulation

Anti-cancer

NCP07 potently inhibits the proliferation of wild-type MCF-7 breast cancer cells with an IC₅₀ of 0.25 μM; it potently inhibits the proliferation of endocrine-resistant LCC2 breast cancer cells with an IC₅₀ of 1.01 μM; and it potently inhibits the proliferation of ESR1-mutant MCF-7^EGFR, MCF-7^D538G and MCF-7^Y537S breast cancer cells, with IC₅₀ values ranging from 0.13 to 1.22 μM^[1].
NCP07 (5-10 μM; 24 h) selectively degrades ERα in wild-type MCF-7 breast cancer cells^[1].
NCP07 (1-10 μM; 24 h) selectively degrades ERα in endocrine-resistant LCC2 breast cancer cells in a concentration-dependent manner^[1].
NCP07 (1-10 μM; 12 h) selectively degrades ERα in a concentration-dependent manner in T47D breast cancer cells as well as ESR1-mutated MCF-7^EGFR, MCF-7^D538G and MCF-7^Y537S breast cancer cells^[1].
NCP07 (5 μM) induces ERα degradation in endocrine-resistant LCC2 breast cancer cells via specific binding to the ERα coactivator binding site (CBS); it can induce the formation of a stable ERα-NCP07-VHL ternary complex in endocrine therapy-resistant LCC2 breast cancer cells through specific binding to ERα CBS^[1].

Anti-cancer

Apoptosis

NCP07 (0.1-20 μM; 72 h) induces apoptosis in endocrine-resistant LCC2 breast cancer cells in a concentration-dependent manner^[1].
NCP07 (1-10 μM; 72 h) activates the apoptotic signaling pathway in endocrine-resistant LCC2 breast cancer cells, inducing caspase-3 activation and PARP cleavage^[1].

Anti-cancer

Cell Cycle Regulation

NCP07 (1-20 μM; 48 h) selectively induces G1-phase cell cycle arrest in endocrine-resistant LCC2 breast cancer cells in vitro in a concentration-dependent manner^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Western Blot Analysis^[1]

Cell Line:

wild-type MCF-7 breast cancer cells
Concentration:

5, 10 μM
Incubation Time:

24 h
Result:

Induced ~20% degradation of ERα at 5 μM.
Induced ~75% degradation of ERα at 10 μM.

Western Blot Analysis^[1]

Cell Line:

endocrine-resistant LCC2 breast cancer cells
Concentration:

1, 5, 10 μM
Incubation Time:

24 h
Result:

Induced degradation of ERα.

Western Blot Analysis^[1]

Cell Line:

ESR1-mutated breast cancer cells (MCF-7^EGFR, MCF-7^D538G, MCF-7^Y537S) and T47D breast cancer cells
Concentration:

1, 5, 10 μM
Incubation Time:

12 h
Result:

Induced graded ERα degradation in four cell strains: T47D (60/80/90%), MCF-7^EGFR (50/70/80%), MCF-7^D538G (30/50/70%), MCF-7^Y537S (20/40/60%) at 1, 5, 10 μM.

Immunofluorescence^[1]

Cell Line:

endocrine-resistant LCC2 breast cancer cells
Concentration:

10 μM (NCP07); 5 μM (E2 co-incubated); 3 μM (KP1490 co-incubated)
Incubation Time:

12 h
Result:

Induced significant co-localization of ERα and VHL (orange-yellow merged fluorescence) in the nucleus.
Co-incubation with KP1490 inhibited ERα-VHL co-localization.
Co-incubation with E2 did not inhibit ERα-VHL co-localization.

Apoptosis Analysis^[1]

Cell Line:

endocrine-resistant LCC2 breast cancer cells
Concentration:

0.1, 1, 10, 20 μM
Incubation Time:

72 h
Result:

Induced concentration-dependent apoptosis in LCC2 cells.

Western Blot Analysis^[1]

Cell Line:

endocrine-resistant LCC2 breast cancer cells
Concentration:

1, 5 μM (PRAP)
1, 5, 10 μM (Caspase-3)
5 μM (cleaved forms)
Incubation Time:

72 h
Result:

Induced concentration-dependent reduction in full-length PARP protein levels.
Induced concentration-dependent reduction in full-length caspase-3 protein levels.
Induced corresponding concentration-dependent increases in cleaved-PARP levels.
Induced corresponding concentration-dependent increases in cleaved-caspase-3 levels.

Cell Cycle Analysis^[1]

Cell Line:

wild-type MCF-7 and endocrine-resistant LCC2 breast cancer cells
Concentration:

1, 10, 20 μM
Incubation Time:

48 h
Result:

Showed no significant effect on cell cycle distribution in MCF-7 cells.
Induced concentration-dependent G1 phase arrest in LCC2 cells.
At 20 μM, 87.80% of LCC2 cells were in G1 phase.

In Vivo

NCP07 (500 mg/kg; single administration) exhibits favorable in vivo safety, with no adverse reactions or body weight changes detected^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Related Protocols :

Chemical Information

Molecular Weight 1121.30
Formel C₅₈H₇₂N₈O₁₃S
SMILES

C[C@@H](C1=CC=C(C2=C(C)N=CS2)C=C1)NC([C@H](C[C@@H](O)C3)N3C([C@H](C(C)(C)C)NC(CCCNC(C(C=C4)=CC(OCC(C)C)=C4NC(C(C=C5)=CC(OCC(C)C)=C5NC(C6=CC(OCCO)=C([N+]([O-])=O)C=C6)=O)=O)=O)=O)=O)=O
Versand

Room temperature in continental US; may vary elsewhere.
Speicherung

Please store the product under the recommended conditions in the Certificate of Analysis.

Reinheit & Dokumentation

Handling Instructions (2659 KB)

Verweise

[1]. Liang J, et al. NCP07: A potent ERα CBS-targeted degrader with dual-action against ESR1 mutations in breast cancer. European journal of medicinal chemistry. 2026 Jun 30;317:119113. [Content Brief]

Calculators

Molaritätsrechner

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Konzentration Konzentration

Volumen Volumen

Molecular Weight Molecular Weight

Verdünnungsrechner

Konzentration _{(Stammlösung)} × Volumen _{(Stammlösung)} = Konzentration _{(Ziellösung)} × Volumen _{(Ziellösung)}

Konzentration _{(Stammlösung)} Konzentration _{(Stammlösung)}

Volumen _{(Stammlösung)} Volumen _{(Stammlösung)}

Konzentration _{(Ziellösung)} Konzentration _{(Ziellösung)}

Volumen _{(Ziellösung)} Volumen _{(Ziellösung)}

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

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MOQ

Minimum order quantity

100 mg

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Biologische Aktivität
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NCP07

Alle PROTACs Isoform-spezifische Produkte anzeigen

Alle Estrogen Receptor/ERR Isoform-spezifische Produkte anzeigen

Biologische Aktivität

Beschreibung

IC50 & Target

In Vitro

In Vivo

Chemical Information

Reinheit & Dokumentation

Verweise

Calculators

Help & FAQs

NCP07 Related Classifications

HY-187225 Related Classifications

Bioz

Keywords

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